Why an Oscar Win Could Mean a Longer Life

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Here's another reason to root for your favorite actor Sunday night: A win might come not just with a golden trophy, but with a longer life.

[50 Ways to Improve Your Finances in 2012]

Oscar winners, it turns out, live an average of 3.6 years longer than nominees who go home empty-handed. That echoes broader findings that suggest rich people live longer; that trend appears to hold true even among celebrities.

The Oscar winner-longevity connection was first noticed by researchers Donald A. Redelmeier and Sheldon M. Singh and published in 2001 paper. Redelmeier told the New York Times that he decided to investigate whether Oscar winners lived longer after watching the awards and noticing that the celebrities "don't look anything like the patients I see in clinic?It's not just the makeup and the plastic surgery and wardrobe. It's the way they move, it's their gestures. They seem so much more vivacious. It seemed so much more than skin-deep and might go all the way to longevity."

To explore whether his hunch was correct, Redelmeier identified more than 1,649 performers, including those nominated for academy awards and cast members of the same gender and similar age who appeared in the same films as the nominees. After examining the performers' life spans, the study found that Oscar winners lived an average of 3.9 years longer than similar performers who were not nominated. As compared to nominees, Oscar winners had a similar longevity boost: On average, winners lived 3.6 years longer than nominees. (The most common cause of death among all performers was heart disease.)

To explain their findings, Redelmeier and Singh suggest that Oscar winners feel pressure to preserve their image, which could lead to healthier behavior. (Of course, celebrity pressure can also have the reverse effect and lead to very public downfalls.) Oscar winners are also likely to benefit from managers, trainers, personal chefs, and other support staff that help them live a healthy lifestyle. The researchers conclude, "The main implication is that higher status may be linked to lower mortality rates even at very impressive levels of achievement."

[Do Rich People Live Longer?]

Since this much-cited study first came out, other researchers have poked holes in its statistical validity, suggesting that the actual longevity boost from an Oscar win might just be one year, and a statistically-insignificant one at that, but Redelmeier continues to explore success-longevity connections among high performers.

In fact, Redelmeier and Singh have also since studied Oscar nominees for best screenplay, and came up with the reverse findings: Winners had a lower life expectancy than nominees, and could expect to live 3.6 years less than their non-winning counterparts. One possible reason is the different type of lifestyle required for writing screenplays. In other words, while actors spend time working out and eating well, writers are often hunched over their computers pounding out words. Similarly, Redelmeier found that medical students who served as class presidents died an average of 2.4 years earlier than their non-presidential classmates. Again, Redelmeier suggests a stressful lifestyle--one that includes taking on a lot of responsibility--could make the difference.

The Oscar-longevity connection is just one more reason be happy for the winners Sunday night.

Twitter: @alphaconsumer

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Why an Oscar Win Could Mean a Longer Life

Sirtuin protein linked to longevity in mammals

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At last, a member of the celebrated sirtuin family of proteins has been shown to extend lifespan in mammals — although it’s not the one that has received the most attention and financial investment.

Sirtuin genes and the proteins they encode have intrigued many researchers who study ageing ever since they were first linked to longevity in yeast. Results published today in Nature suggest that the overexpression of one gene, called sirtuin 6 (SIRT6), can lengthen lifespan in male mice by as much as 15.8%1.

Male mice with boosted levels of the sirtuin protein SIRT6 could live longer.

Getty Images

For years, another member of the family, SIRT1, has hogged much of the spotlight because it is the mammalian member of the sirtuin clan most closely related to the longevity-linked yeast gene. Some researchers speculated that SIRT1 may also boost lifespan in mammals, and that it was the target of resveratrol, a compound found in red wine that had been linked to a variety of health benefits. 

Sirtuin fervour reached its height in 2008, when the London-based drug company GlaxoSmithKline paid US$720 million for a biotechnology company that was initially focused on finding SIRT1-activating compounds as possible treatments for type 2 diabetes. But since then, results suggesting that SIRT1 affects lifespan in the fruitfly Drosophila melanogaster and the nematode Caenorhabditis elegans have been questioned (see Longevity genes challenged). And no effect of SIRT1 on longevity in mammals has been reported, although its expression is associated with a healthier metabolism in mice fed a high-fat diet.

Amid the excitement about SIRT1, it was in part the relative obscurity of SIRT6 that drew molecular biologist Haim Cohen of Bar-Ilan University in Ramat-Gan, Israel, to study the gene. “People were mostly interested in SIRT1,” he says. “So I thought it might be better for us as a new lab to work on something that is less crowded.”

A new pathway

In 2006, researchers had reported that mice lacking SIRT6 seemed to age more quickly2. The mice were small and sickly, had a reduced capacity to repair damaged DNA, and died a month after birth.

Cohen and his colleagues decided to find out what would happen if mice expressed higher levels of the SIRT6 protein than normal. They found that longevity in female mice was unaffected by the excess protein, but that the median lifespan of male mice rose by 14.5% in one line of their transgenic mice and 9.9% in another1.

Another measure of longevity, maximum lifespan (generally more valued by researchers into ageing because it is less likely to be affected by other factors such as changes in infant mortality), rose by 15.8% in the first line of mice, and 13.1% in the second, although the latter increase was not statistically significant.

Furthermore, in the transgenic mice, levels of proteins involved in the 'insulin-like growth factor 1' pathway, which has been previously linked to longevity, were also affected by SIRT6 expression.

Critical caveats

The results are interesting, and the magnitude of lifespan extension is impressive, says Richard Miller, who studies ageing at the University of Michigan in Ann Arbor. But the work must be interpreted with care, he adds. “It’s a good bet that each of the sirtuins does something interesting,” says Miller. “But the case for whether any one of them is important to ageing and longevity in mammals is somewhat weak and circumstantial.”

The strain of mice used in the study is particularly prone to tumours, especially in males, says Miller. It’s possible, then, that the longer lifespans could be the result of an anti-cancer effect of SIRT6 rather than a direct effect on ageing.

Cohen acknowledges that this is a possibility, but notes that statistical analyses found no evidence that differences in tumour rates were contributing to the longevity effects of SIRT6.

David Lombard, a sirtuin researcher at the University of Michigan agrees with Miller, saying that it is important for researchers to directly address whether SIRT6 affects several of the conditions associated with ageing, such as cataract formation and declines in memory and mobility. Since the initial work with SIRT6-deficient mice was published, he notes, researchers have found that much of what initially seemed to be an accelerated rate of age-related degeneration may in fact be attributable to metabolic defects that cause extremely low blood-sugar levels.

And why does SIRT6 affect males and females differently? Cohen’s lab is trying to piece that together, but for now he can only offer speculation. He notes that in the strain of mice his team used, females live about 15% longer than males and that overexpression of SIRT6 simply allowed the males to catch up to the females. Perhaps, then, SIRT6 is mimicking effects already seen in the females of this strain of mice. In this context, Rafael de Cabo, who studies ageing at the National Institute on Ageing in Baltimore, Maryland, notes that the expression of some proteins in the transgenic mice producing excess SIRT6 matched the expression of those proteins in normal, control female mice.

The new focus on SIRT6 does not mean that the other sirtuins have been left by the wayside, says Miller. Researchers are beginning to look at the effects of SIRT1 when expressed in specific tissues, and work on the other members of the family is continuing apace. “People are just beginning to come to grips with the fact that there are seven sirtuins and each may do different things,” says Miller. “The quicker people stop thinking in terms of ‘it’s either gold or tin’ and start addressing the nuances of sirtuin function, the better.”

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Sirtuin protein linked to longevity in mammals

Sirtuin Protein Linked to Longevity in Mammals for First Time

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By Heidi Ledford of Nature magazine

At last, a member of the celebrated sirtuin family of proteins has been shown to extend lifespan in mammals -- although it's not the one that has received the most attention and financial investment.

Sirtuin genes and the proteins they encode have intrigued many researchers who study ageing ever since they were first linked to longevity in yeast. Results published today in Nature suggest that the overexpression of one gene, called sirtuin 6 (SIRT6), can lengthen lifespan in male mice by as much as 15.8%.

For years, another member of the family, SIRT1, has hogged much of the spotlight because it is the mammalian member of the sirtuin clan most closely related to the longevity-linked yeast gene. Some researchers speculated that SIRT1 may also boost lifespan in mammals, and that it was the target of resveratrol, a compound found in red wine that had been linked to a variety of health benefits.

Sirtuin fervor reached its height in 2008, when the London-based drug company GlaxoSmithKline paid US$720 million for a biotechnology company that was initially focused on finding SIRT1-activating compounds as possible treatments for type 2 diabetes. But since then, results suggesting that SIRT1 affects lifespan in the fruitfly Drosophila melanogaster and the nematode Caenorhabditis elegans have been questioned (see Longevity genes challenged). And no effect of SIRT1 on longevity in mammals has been reported, although its expression is associated with a healthier metabolism in mice fed a high-fat diet.

Amid the excitement about SIRT1, it was in part the relative obscurity of SIRT6 that drew molecular biologist Haim Cohen of Bar-Ilan University in Ramat-Gan, Israel, to study the gene. "People were mostly interested in SIRT1," he says. "So I thought it might be better for us as a new lab to work on something that is less crowded."

A new pathway

In 2006, researchers had reported that mice lacking SIRT6 seemed to age more quickly. The mice were small and sickly, had a reduced capacity to repair damaged DNA, and died a month after birth.

Cohen and his colleagues decided to find out what would happen if mice expressed higher levels of the SIRT6 protein than normal. They found that longevity in female mice was unaffected by the excess protein, but that the median lifespan of male mice rose by 14.5% in one line of their transgenic mice and 9.9% in another.

Another measure of longevity, maximum lifespan (generally more valued by researchers into ageing because it is less likely to be affected by other factors such as changes in infant mortality), rose by 15.8% in the first line of mice, and 13.1% in the second, although the latter increase was not statistically significant.

Furthermore, in the transgenic mice, levels of proteins involved in the 'insulin-like growth factor 1' pathway, which has been previously linked to longevity, were also affected by SIRT6 expression.

Critical caveats

The results are interesting, and the magnitude of lifespan extension is impressive, says Richard Miller, who studies ageing at the University of Michigan in Ann Arbor. But the work must be interpreted with care, he adds. "It's a good bet that each of the sirtuins does something interesting," says Miller. "But the case for whether any one of them is important to ageing and longevity in mammals is somewhat weak and circumstantial."

The strain of mice used in the study is particularly prone to tumors, especially in males, says Miller. It's possible, then, that the longer lifespans could be the result of an anti-cancer effect of SIRT6 rather than a direct effect on ageing.

Cohen acknowledges that this is a possibility, but notes that statistical analyses found no evidence that differences in tumor rates were contributing to the longevity effects of SIRT6.

David Lombard, a sirtuin researcher at the University of Michigan agrees with Miller, saying that it is important for researchers to directly address whether SIRT6 affects several of the conditions associated with ageing, such as cataract formation and declines in memory and mobility. Since the initial work with SIRT6-deficient mice was published, he notes, researchers have found that much of what initially seemed to be an accelerated rate of age-related degeneration may in fact be attributable to metabolic defects that cause extremely low blood-sugar levels.

And why does SIRT6 affect males and females differently? Cohen's lab is trying to piece that together, but for now he can only offer speculation. He notes that in the strain of mice his team used, females live about 15% longer than males and that overexpression of SIRT6 simply allowed the males to catch up to the females. Perhaps, then, SIRT6 is mimicking effects already seen in the females of this strain of mice. In this context, Rafael de Cabo, who studies ageing at the National Institute on Ageing in Baltimore, Maryland, notes that the expression of some proteins in the transgenic mice producing excess SIRT6 matched the expression of those proteins in normal, control female mice.

The new focus on SIRT6 does not mean that the other sirtuins have been left by the wayside, says Miller. Researchers are beginning to look at the effects of SIRT1 when expressed in specific tissues, and work on the other members of the family is continuing apace. "People are just beginning to come to grips with the fact that there are seven sirtuins and each may do different things," says Miller. "The quicker people stop thinking in terms of `it's either gold or tin' and start addressing the nuances of sirtuin function, the better."

This article is reproduced with permission from the magazine Nature. The article was first published on February 22, 2012.

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Sirtuin Protein Linked to Longevity in Mammals for First Time

Longevity Is for the Young, Too

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Longevity has been one of the great success stories of the past few decades. Miracle drugs, better healthcare, and improved lifestyles have combined to add many years to average life spans. For people who take good care of themselves and do not have adverse family health histories, living well into their 90s is held out as the norm, not the exception.

[In Pictures: The 10 Best Places to Retire in 2012.]

Some of the attention on longevity has been precautionary. The financial services industry, for example, has been beating the drum to raise concerns that people will live so long that they will risk running out of money before they die. Of course, investment firms are more than happy to help people map out better retirement programs.

There also have been concerns that an aging society will tax Social Security and Medicare. Living longer has also been associated with enduring longer periods of coping with chronic illnesses (especially Alzheimer's) and an extended stage of frailty.

But the longevity story is mostly positive. And as gains in life spans have moved from being oddities to mainstream expectations, they are helping to trigger reassessments of how people should be using their "extra" years.

An assumption that the benefit of longer lives will consist simply of longer retirements and added years on the sidelines of life is being joined, and in some cases supplanted, by the notion that many of these years can be used to expand and enrich earlier stages of life.

Younger Americans are taking longer to hit major developmental milestones--more time to complete college, longer periods to settle down, and later ages for marriage and parenthood. The tough economy is responsible for some of these extended paths, but these are longer-term trends as well.

[See Do You Face 'Money Death' in Old Age?]

Sociologist Eric Klinenberg recently wrote Going Solo, a book about the growing numbers of Americans of all ages who are choosing to live alone. "The Stanford sociologist Michael Rosenfeld argues that middle-class people in their twenties and thirties now look forward to a 'second adolescence.'" Klinenberg writes, "in which they seek out new experiences--from serial dating to interracial and same-sex relationships--and refrain from commitment unless they find their 'true romantic love.'"

The U.S. Census Bureau says the age of a person's first marriage is now the highest since records began in the 19th century: 28.7 years for men in 2011, and 26.5 years for women, on average.

The median age at which women have their first child was above 25 for the first decade of the 21st century, the Census Bureau reported. But this median obscures some divergent trends. Married couples with college degrees are holding off on marriage and parenthood even longer. Further, career women are often deciding to wait until they've solidly established their positions before deciding to have children. Accordingly, the number of women having babies while in their late 30s and 40s has been rising steadily.

While many younger people are allowing their developmental timetables to stretch out, there is mostly anecdotal research that they have done so because of any heightened awareness of extended life spans. However, there is stronger evidence that older Americans are very conscious that the clock may end up ticking a lot longer for them.

More and more older employees are keeping their jobs and staying in the workforce. While the recession gets much credit for this trend, it predates the downturn. For financial and lifestyle reasons, people have been deferring traditional retirements in growing numbers for years.

The percentage of Americans in the workforce who are age 55 or older "has been rising steadily since 1993, when it stood at 29.4 percent," the Employee Benefit Research Institute (EBRI) recently reported. This group's labor-force participation rate reached 40.2 percent in 2010 and stayed there in 2011.

[See 6 Tips for Evaluating Longevity Insurance.]

"For men age 55 and older, the labor force participation rate grew from 1975 to 2010, before flattening out or slightly decreasing to 46.3 percent," EBRI said. "Among women age 55 and older, the labor force participation rate grew from 22.8 percent in 1993 to 35.1 percent in 2010, its highest level, where it remained in 2011."

These high rates are also linked with rising numbers of older people who not only continue to work but have decided to reinvent their professional lives while in their 60s and 70s. Marc Freedman, founder of Civic Ventures and its employment offshoot, Encore Careers, makes a compelling case that we are in the process of creating a new stage of life between middle age and old age.

Sociologist Laura Carstensen, director of the Stanford Center on Longevity and author of A Long Bright Future, has championed adding years to earlier stages of life. People face stressful and regretful time deficits at some earlier stages of life, she notes. Early career development and parenthood come to mind as stages where we'd all like more time. In our later years, however, some people have so much extra time that it can amount to too much of a good thing, leading to boredom and loneliness.

Wouldn't it be nice, Carstensen says, if we could "exchange speeding through life for a chance to enjoy the journey."

Twitter: @PhilMoeller

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Longevity Is for the Young, Too

Conn. bill looks to add labels to engineered food

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HARTFORD, Conn. (AP) — Consumers at Connecticut grocery stores would be able to know if genetically engineered foods are in the merchandise mix under a bill state lawmakers are considering to require the labeling of such foods.

Neither the federal government nor any state currently has a labeling requirement that applies to all genetically modified foods. Connecticut is among nearly 20 states considering a labeling mandate amid health concerns that supporters of the legislation have raised about such foods.

Connecticut's legislation would require clear labeling on any food sold in the state that is completely or partially produced with genetic engineering.

Rep. Richard Roy, D-Milford, said he introduced the legislation due to public concern over the issue. Roy co-chairs the state Environment Committee, which heard from supporters and opponents of the bill at a hearing Wednesday.

Roy said his bill has gained bipartisan support, and he expects the committee to pass it, although its fate after is unclear.

"We're not taking a stance on whether GMOs (genetically modified organisms) are good or bad," said Roy. "What we're saying is that we have a right to know what we're putting in our bodies."

Proponents of the legislation say that genetically engineered foods pose allergy and other health risks and that the labels will increase safety for consumers.

Analiese Paik, who runs the Fairfield Green Food Guide website and testified in favor of the labels, said that the Food and Drug Administration has yet to produce a scientific study on whether or not genetically modified foods are safe.

Paik pointed to a recent Canadian study that found toxins from genetically engineered corn circulating in the bloodstream of women.

"The burden of proof is on the FDA to prove that it's safe," she said.

U.S. Department of Agriculture spokesman R. Andre Bell, said the USDA, FDA and Environmental Protection Agency regulate genetically engineered crops to ensure they are safe to eat and grow.

Opponents of the proposed legislation, including grocery stores and farmers, say they disagree with Paik's claims and argue that genetically engineered food has been long-studied and is proven to be safe.

Brian Kennedy, a spokesman from the Grocery Manufacturers Association, said in a statement that "a special declaration on the food label would...not provide any additional useful information."

FDA spokeswoman Siobhan DeLancey said that genetically modified foods, as a class, pose no greater health risks than traditional foods. She said that genetically modified crops must meet regulatory standards and may undergo a voluntary consultation to ensure they are safe.

DeLancey said that while there are currently no genetically modified animal-based products on the market, they undergo substantial testing to ensure they are safe, as well.

She said the FDA has the authority to label products only when there is a material difference affecting things like nutritional values.

Henry Talmage, executive director of the Connecticut Farm Bureau, said that adding labels to genetically engineered foods would be costly for farmers and complicate selling products over state lines. He said that organic and GMO-free certified farmers currently have the option to label their products as such, making the bill's mandatory label proposal redundant.

While the legislation looks to add labels, it does not require genetically engineered ingredients to be listed or identified. Additionally, the label would not be placed on foods from animals that were fed genetically engineered crops or fast food.

Under the proposed legislation, genetically engineered foods include any food that is unnaturally produced by altering genetic material.

Growing genetically engineered crops is attractive to farmers because they are modified to resist insects and tolerate herbicides. According to USDA data, the growth of genetically engineered crops has increased tremendously since their commercial introduction in 1996.

Between 1996 and 2011, growth rates for genetically engineered soybeans that are herbicide tolerant rose from less than 10 to 94 percent. Likewise, the rates for genetically engineered cotton and corn have risen around 70 percent across the board.

In recent years, many states have pushed to require clear labeling of genetically engineered products. Earlier this month, a California bill calling for labeling of genetically engineered salmon narrowly failed to pass a committee vote.

Connecticut is among 18 states that are considering labeling requirements for genetically modified foods, said Scott Hendrick, a spokesman for the National Conference of State Legislatures. He said Massachusetts, New York, Rhode Island, Vermont and New Hampshire are among surrounding states that are currently considering similar legislation.

Although no states require all genetically engineered food to be labeled, Alaska has a law requiring the labeling of genetically engineered fish, Hendrick said.

At the federal level, Congress is reviewing legislation in both the House of Representatives and Senate requiring labels on genetically engineered fish. The House is also reviewing legislation that calls for mandatory labeling of all genetically modified foods.

Connecticut Gov. Dannel P. Malloy's office is reviewing the legislation, his spokesman, Andrew Doba, said.

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Conn. bill looks to add labels to engineered food

Can consuming caffeine while breastfeeding harm your baby?

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Public release date: 21-Feb-2012
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Contact: Cathia Falvey
cfalvey@liebertpub.com
914-740-2100
Mary Ann Liebert, Inc./Genetic Engineering News

New Rochelle, NY, February 21, 2012?Babies are not able to metabolize or excrete caffeine very well, so a breastfeeding mother's consumption of caffeine may lead to caffeine accumulation and symptoms such as wakefulness and irritability, according to an interview with expert Ruth Lawrence, MD, published in Journal of Caffeine Research, a peer-reviewed journal from Mary Ann Liebert, Inc. The interview is available on the Journal of Caffeine Research website at http://www.liebertpub.com/jcr.

Caffeine is found in a wide range of products in addition to coffee, tea, and chocolate, including soft drinks, sports drinks, and some over-the-counter medications.

In a provocative discussion with Dr. Ruth Lawrence, Department of Pediatrics, University of Rochester School of Medicine and Dentistry, Jack E. James, PhD, Editor-in-Chief of Journal of Caffeine Research, asks a variety of probing questions. Is there a safe level of caffeine intake while breastfeeding? Are there potential long-term effects of caffeine exposure on development and intellect? Can a baby whose mother consumed caffeine during pregnancy experience withdrawal if she then abstains from caffeine while breastfeeding? Dr. Lawrence bases her responses on the scientific and medical evidence related to caffeine exposure in breastfed babies, and distinguishes between what is and what is not well understood in this developing field of study.

"Usually a mother, particularly if she is breastfeeding, is cautioned to limit her caffeine intake," says Dr. Lawrence, who is Editor-in-Chief of the peer-reviewed journal Breastfeeding Medicine. After giving birth, mothers "should consume all things in moderation and try to avoid the excesses that might really add up to a lot of caffeine."

###

About the Journal

Journal of Caffeine Research: The International Journal of Caffeine Science is a quarterly peer-reviewed journal published in print and online that covers the effects of caffeine on a wide range of diseases and conditions, including mood disorders, neurological disorders, cognitive performance, cardiovascular disease, and sports performance. The Journal explores all aspects of caffeine science including the biochemistry of caffeine; its actions on the human body; benefits, dangers, and contraindications; and caffeine addiction and withdrawal, across all stages of the human life span from prenatal exposure to end-of-life. Tables of content and a free sample issue may be viewed on the Journal of Caffeine Research website at http://www.liebertpub.com/jcr.

About the Company

Mary Ann Liebert, Inc. is a privately held, fully integrated media company known for establishing authoritative peer-reviewed journals in many promising areas of science and biomedical research, including Breastfeeding Medicine, Journal of Medicinal Food, and Journal of Child and Adolescent Psychopharmacology. Its biotechnology trade magazine, Genetic Engineering & Biotechnology News (GEN), was the first in its field and is today the industry's most widely read publication worldwide. A complete list of the firm's 70 journals, books, and newsmagazines is available online at http://www.liebertpub.com.

Mary Ann Liebert, Inc. 140 Huguenot Street, New Rochelle, NY 10801-5215 http://www.liebertpub.com
Phone (914) 740-2100 (800) M-LIEBERT Fax (914) 740-2101

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Can consuming caffeine while breastfeeding harm your baby?

'DNA Origami' nanorobots hunt and kill cancer cells

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Researchers from Harvard University in the United States have built "DNA origami" nanorobots to hunt down and destroy cancer cells in the body.

The nanorobots can transport payloads such as drug molecules and antibodies to specific cells of the body, tech site Technorati reported.

"We can finally integrate sensing and logical computing functions via complex, yet predictable, nanostructures — some of the first hybrids of structural DNA, antibodies, aptamers and metal atomic clusters — aimed at useful, very specific targeting of human cancers and T-cells," Technorati quoted George Church, Ph.D., a Wyss core faculty member and Professor of Genetics at Harvard Medical School who is Principal Investigator on the project, as saying.

The report said the scientists used “DNA origami” to develop the containers with folded DNA chains.

Aptamers were used to lock the barrel-shaped robot and to recognize specific cell types.

Researchers used these robots in different cultures of cancerous cells such as leukemia and lymphoma, and found the unlocking of the robots occurred on contact with the cancer cell proteins.

This led to the release of antibodies that stopped the growth of the cancer cells.

"Although the robots caused some problems of toxicity but those problems were less than most of the chemicals and materials would have," Technorati said.

A separate article on tech site Mashable said the study was published in Science on Thursday. Its researchers - Shawn Douglas, Ido Bachelet, and Church - are all affiliated with Harvard University’s Wyss Institute for Biologically Inspired Engineering.

Douglas developed the open-source software the researchers used called Cadnano to design the structures.

It said the nanorobots mimic a cell’s receptor system to communicate with cells.

Once the nanorobot detects the cells it is looking for, it will spring into action.

Each nanobot can hold molecules to be delivered to cells. On the outside of the nanobots would be two strands that could help recognize target cells, and release their contents at the right time.

While the system has yet to be tested in living organisms, the researchers are considering testing the nanorobots in mice. — TJD, GMA News

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'DNA Origami' nanorobots hunt and kill cancer cells

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DNA links accused to crime scene

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DNA links accused to crime scene

Posted in DNA

Victims Urge Georgia to Improve Funding for Forensic DNA

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ATLANTA, Feb. 22, 2012 /PRNewswire/ -- Victims of crimes and their families met to discuss the need for immediate action in support of better funding for the Georgia forensic DNA program.   Debbie Smith, an outspoken rape survivor and namesake of the federal Debbie Smith DNA Backlog Elimination Act, was joined by Jayann Sepich, mother of murder victim Katie Sepich, namesake of Katie's Law -- both in Atlanta to meet with the parents of murder victim Johnia Berry (Mike and Joan Berry) and Savanna rape victim Susan Cash.  The Georgia Network to End Sexual Assault (GNESA) hosted the discussion of the importance of federal funding in reducing Georgia's backlog of unsolved cases, and the dire need for the State to provide improved funding for its DNA program.   

GNESA's Executive Director, Jennifer Bivins, noted that Georgia's DNA program provides victims with an important step forward in their healing process when attackers are named through DNA.  But Georgia's commitment to state funding pales in comparison with that of other state labs, currently represented in Atlanta at the AAFS meeting, as most states in the country provide significantly stronger support for their DNA analysts.  Mrs. Smith declared, "It is so important for DNA labs to receive adequate state funding.  The public safety of their residents relies on it." 

The Berrys have lobbied for several years for a law to improve the state DNA database program.  "Every year we've been told that this bill is not feasible until the DNA program is better funded.  Every year we come back, and the lab is no better funded.  Enough is enough.  We need to do everything possible to fix this situation.  Crime victims in Georgia deserve better, and we know our state legislators will agree."

Mrs. Cash (whose 1985 rape is pending a specialized DNA test) noted that Georgia has a strong history with DNA, "But it would be an injustice to victims if this backlog money is used not to improve backlogs but merely to keep the Georgia DNA program afloat.  Our forensic experts deserve better treatment.  Our victims deserve better."  Ms. Sepich agreed, "Studies show that investing in DNA is worth it.  Forget the lives that can be saved – the city of Denver found a $90 return on investment for every dollar spent on DNA.  How much money is Georgia losing by not making this investment?"

Mrs. Smith closed by pleading, "The federal money was never meant to replace the state's responsibility to its victims and other citizens.  To ignore the basic personnel needs of this program undermines the important strides forward that we have made with DNA and allows backlogs to build, criminal cases to remain unsolved, victims to remain in fear of their unknown attacker, and those attackers to remain on the streets."

 

 

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Posted in DNA

DNA helps identify skull as missing man's

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CONROE, Texas -

Detectives need help to solve the death of a man who disappeared in 1984.

Montgomery County sheriff's deputies said George "Bud" Sager, 30, withdrew money from his bank on Interstate 45 near Spring Cypress Road on June 7, 1984. Investigators said Sager planned to use the money to pay for closing costs on a home.

Sager was never seen or heard from again.

Deputies said that it appeared that Sager had never been officially listed as missing. In January 2010, Sager's sister contacted investigators and the cold case squad opened an investigation. DNA from his family was collected and entered into the Combined DNA Index System.

Cold case detectives learned that someone collecting cans along F.M. 1375 about a mile west of Interstate 45 in Walker County on Dec. 18, 1989, found a human skull on the side of the road. There was a handwritten note with the skull indicating that it had been found in the woods, but the person who found it did not want to be involved in the investigation.

The skull was sent to the Harris County Medical Examiner's Office, but a cause of death could not be determined. When DNA technology began to be used in unidentified remains cases, DNA was collected from the skull and entered into the Combined DNA Index System.

In October 2011, after Sager's relatives' DNA had also been entered into the Combined DNA Index System, there was a match to the skull. It was positively identified as Sager's.

Investigators said they do not know how Sager died, but suspect foul play may be involved. He may have been the victim of a robbery, detectives said. Sager's pickup truck was found abandoned in the parking lot of the Crossroads shopping center on Interstate 45 near Highway 105 in Conroe on July 3, 1984. Detectives said there was no evidence in the pickup truck that gave them any leads.

Cold case detectives said they want to talk to the person who found the skull, or anyone else who may have information about Sager's death. Anyone with information is asked to call detectives at 281-297-6510.

Investigators also urged anyone with a relative who has been missing for a long period of time to contact the investigating law enforcement agency to be certain that the person is entered in the national missing person's database. They also recommend exploring the possibility of collecting DNA to be entered into the Combined DNA Index System.

Copyright 2012 by Click2Houston.com. All rights reserved. This material may not be published, broadcast, rewritten or redistributed.

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DNA found under nails

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WORCESTER —  A partial DNA profile generated from the fingernail scrapings of Clara J. Provost matched the DNA of Ronald D. Dame, the man accused of murdering her 38 years ago, a Worcester Superior Court jury was told yesterday.Calin L. Drugan, a chemist and DNA analyst at the state police crime lab, testified at Mr. Dame?s trial that genetic testing she conducted in 2007 showed Mr. Dame?s DNA profile matched a profile derived from material removed from beneath the fingernails of Ms. Provost?s right hand after she was found slain in her apartment at 13 Highland Ave. in Fitchburg Jan. 7, 1974.

Prosecutors allege the 23-year-old woman, whose throat was slashed, was killed by the now 65-year-old Mr. Dame after he broke into her apartment with the intention of forcing her to have sex with him.

Assistant District Attorney Joseph A. Quinlan told the jury in his opening statement that he expected the evidence to show Ms. Provost scratched the left side of Mr. Dame?s face with the fingernails of her right hand during the attack. Police saw the scratches when they questioned him later that day, according to the assistant district attorney.

Mr. Dame?s lawyer, John H. LaChance, told the jury in his opening statement that Mr. Dame was at his sister?s house when Ms. Provost was killed and that one of Mr. Dame?s nieces scratched him as he was tickling her.

Ms. Drugan testified that the chances of the DNA match occurring at random were one in 2.2 million in the Caucasian population of unrelated males.

She also testified that Mr. Dame?s DNA profile matched a genetic profile derived from sperm and seminal fluid found on a paper towel that police said they found in the back seat of Mr. Dame?s car when he went to the Fitchburg police station for questioning on Jan. 7, 1974.

She said the chances of such a match occurring at random in the non-sperm fraction of the stain on the paper towel were one in 27.8 million in the Caucasian population, and one in 5,227 for the sperm fraction of the stain.

A representative of an independent testing lab testified earlier that the paper towel from Mr. Dame?s car and pieces of paper towel found on Ms. Provost?s kitchen floor were from the same manufacturer and were consistent with being from the same batch or run.

Although investigators had long considered him a suspect in the killing, Mr. Dame was not charged until 2006 when, prosecutors said, DNA evidence linked him to the crime.

Testimony in the trial is scheduled to resume today.

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New Mini DNA Sequencer, Size of a USB Stick, Is Fast and Cheap | 80beats

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For years, the cutting edge technology for DNA sequencing has involved mincing DNA up into tiny pieces. Even as sequencing has gotten faster and cheaper, each new process has relied on chopping the DNA up to be analyzed, because, although this process can introduce errors in the readout and can be expensive, it was still the best we had. Now, technology unveiled at a recent conference in Florida could mean that the age of slicing and dicing is over, thanks to something called a nanopore.

A nanopore is a ring of proteins, made by a bacterium, through which DNA can be threaded, like a string through a bead. In the method of DNA sequencing just debuted by Oxford Nanopore Technologies, long, intact strands of DNA are shunted through nanopores on a chip, and the electrical conductivity of each nucleic acid as it comes through the pore lets scientists tell which DNA “letter” it is—A, T, G, or C. A long strand of DNA analyzed this way, importantly, isn’t destroyed, so it can be reanalyzed, and errors introduced in processes that use chopping are also avoided. Using such basic physical laws to deduce a DNA sequence is a simple, elegant solution to a tough problem. That’s perhaps why nanopore sequencing methods have attracted some significant investment in recent years: the UN National Human Genome Research Institute had, by 2008, given $40 million to groups pursuing nanopore sequencing.

Oxford Nanopore’s presentation featured two devices they hope to start selling later this year: the GridION, which is a heavy-duty lab device that could theoretically sequence a human genome in 15 minutes and which they used to produce a sample viral genome sequence, and the MiniION, which is the size of a USB stick, will cost $900, and should be able to sequence a human genome in 6 hours and tiny viral and bacterial genomes in seconds. That’s very, very fast and very cheap—cheap enough that even curious hobbyists might be able to indulge. An important caveat: Though these devices promise to eliminate the errors brought about by chopping DNA up for analysis, they still currently have an error rate that is four times that of current techniques, perhaps because they still aren’t quite sensitive enough to fulfill nanopore sequencing’s promise, though the coverage of the company’s presentation doesn’t go into detail. But the company plans to have the error rate down to an acceptable level by the time the devices go to market. If Oxford Nanopore can bring accuracy up, and maintain it as they try to sequence larger and larger genomes, DNA sequencing companies with more expensive techniques may be looking at some serious competition.

Scientists are genuinely, if cautiously, excited by what they’ve seen of Oxford Nanopore’s work. “I think it is all credible,” Chad Nusbaum, co-director of the Genome Sequencing and Analysis Program at the Broad Institute in Cambridge, Massachusetts, told Nature News. “I would bet they are even underplaying it because they don’t want to risk overpromising.” For scientists talking about biotech, that’s pretty hopeful phrasing.

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DNA links accused to 1983 murder scene

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Three crime-scene DNA samples have been linked to the man accused of killing and sexually assaulting a retired hairdresser 28 years ago in Petrolia, Ont.

The evidence came from OPP identification officer Darren Soucie, the only witness to testify during the jury trial Wednesday.

The 44-year-old accused is charged with the first-degree murder and sexual assault of Velma Thomson in October, 1983, but cannot be identified under the Youth Criminal Justice Act because he was 15 years old at the time of the slaying.

Samples from Thomson’s pubic hair, along with semen and hairs found on her slipper, were compared to DNA from a blood sample taken after the man was arrested in June 2008.

It's highly probable DNA from the semen found on the pubic hair belongs to the accused, according to a report form the Centre of Forensic Sciences in Toronto, where the DNA analysis was done.

The probability that another unrelated person could have been the DNA donor was set at one in 1.5 quadrillion (1,500,000,000,000,000).

The OPP identification officer presenting the report only submitted the samples and there will be further evidence regarding DNA testing, said Toronto defence lawyer John Norris.

Norris raised no objections during the officer’s testimony, but said the defence’s silence should not be taken as any kind of admission.

Last week jurors heard DNA from chewing gum in the accused man’s garbage was not from the same source as crime scene DNA. That testing compared DNA from the gum and a vagina swab from Thomson.

A re-examination of crime scene exhibits in 2008 found hairs on Thomson’s slipper that had been found adjacent to her body in October 1983.

In 2010 the slipper was sent to the forensic centre to be tested for bodily fluids and DNA analysis.

That testing showed it was highly probable semen DNA on the hairs belonged to the suspect.

The likelihood of another unrelated person being the donor of that DNA was set at one in 51 billion.

Soucie’s testimony about prior exhibit-handling, including the accused man’s blood sample, consumed most of Wednesday’s trial time.

Defence cross-examination, regarding the exhibit-handling, is expected Thursday. The doctor who did the post-mortem examination is also expected to testify.

Thomson had turned 70 a few days before her body was found by a neighbour in the converted garage of her home that had served as a hairdressing salon.

Her throat had been cut and she had an apparent stab wound in her back.

nbowen@theobserver.ca

 

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Telome Health Co-Founder And Nobel Laureate Elizabeth Blackburn Awarded Innovator Of The Year

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Telome Health, Inc.™, a privately held biotechnology company focused on the role of telomere biology in human health, has announced that co-founder and Nobel Laureate Elizabeth Blackburn has been awarded Innovator of the Year by Silicon Valley Business Journal.

Menlo Park, CA (PRWEB) February 23, 2012

Telome Health, Inc.™, a privately held biotechnology company focused on the role of telomere biology in human health, has announced that co-founder and Nobel Laureate Elizabeth Blackburn has been awarded Innovator of the Year by Silicon Valley Business Journal.

"I am very pleased and honored to receive this award, especially coming from the heart of innovation, Silicon Valley, and to acknowledge the efforts of my amazing colleagues” said Dr. Blackburn.

Dr Blackburn is an internationally recognized thought leader and expert on the biology of telomeres. She was awarded the 2009 Nobel Prize in Medicine and Physiology along with Drs. Carol Greider and Jack Szostak for her work in this field. She co-founded Telome Health in 2010 with colleagues Calvin Harley, Elissa Epel and Jue Lin who also recognized experts in the field of telomere biology. Dr. Blackburn is Morris Herzstein Professor of Biology and Physiology at the University of California at San Francisco. She also serves on the Board and is a Scientific Advisory for Telome Health.

“We are thrilled that Dr. Blackburn has been awarded the Innovator of The Year by The Silicon Valley and San Jose Business Journal” noted Daniel Hunt, CEO of Telome Health. “This is just one of the many notable and prestigious awards that she has received for her significant contributions to the field of telomere biology. We are proud to work with Elizabeth to develop a diagnostic test that will further empower individuals and physicians to manage disease risk using a more proactive, personalized approach.”

Telome Health, Inc. is developing a proprietary assay that measures telomere length called the TeloTest™ that it anticipates launching in 2012. Telomeres are repetitive DNA sequences at the ends of human chromosomes that protect them from unraveling similar to the plastic tips (aglets) located on the ends of shoelaces. Research supports that as telomeres get shorter, the chromosome becomes less stable. If this shortening occurs faster than is observed in a normal or healthy population, it may be an indication of stress or other co-morbid factors that have not yet been detected by other tests or actual symptoms.

The TeloTest assay utilizes quantitative polymerase chain assay, also called qPCR, and is the most clinically validated technology used to determine telomere length. “The body of scientific and clinical evidence using qPCR is enormous” said Blackburn. “It is really the technology for which all others should be compared since such studies using this technology conclusively support that negative changes in telomere length is directly associated aging and disease risk.”

Envisaged as being taken annually, the test serves as a “check engine” light that may provide an early warning to individuals and their physicians that further medical assessment or changes in lifestyle habits are warranted.

About Telome Health, Inc.

Telome Health, Inc. is a privately held biotechnology company that is focused on developing proprietary telomere based technologies to diagnose, prevent and treat human disease. Its first product, the TeloTest is anticipated to launch in 2012. The company was co-founded by Elizabeth Blackburn who was awarded the Nobel Prize in Medicine for her scientific contributions in the field of telomere biology and Drs. Calvin Harley, Elissa Epel and Jue Li who are internationally recognized experts in this field. The company is located in Menlo Park, CA.

Contact:

Patricia Sinatra

VP of Corporate Development and Strategy

Telome Health, Inc.

650.289.0289

http://www.telomehealth.com/media/index.html

###

Patricia Sinatra
Telome Health, Inc.
650.289.0289
Email Information

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Telome Health Co-Founder And Nobel Laureate Elizabeth Blackburn Awarded Innovator Of The Year

Chemistry Professor Tao Xu receives CAREER Grant from National Science Foundation

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DeKALB (NIU) -- NIU Professor Tao Xu, who has developed a promising nanoscience research program in solar energy conversion, is now getting a big boost from the National Science Foundation.

NSF has awarded the chemistry and biochemistry professor with a prestigious Faculty Early Career Development (CAREER) grant of $400,000 over the next five years in support of his research and teaching efforts.

CAREER awards support junior faculty who exemplify the role of teacher-scholars through outstanding research, excellent education and the integration of education and research.

“This award is a tribute to the quality and productivity of Dr. Xu and his research group,” said Jon Carnahan, chair of the Department of Chemistry and Biochemistry. “We’re very proud of Tao’s accomplishment.”

Xu also is affiliated with NIU’s Institute for Nano Science, Engineering, and Technology. His research group is working to develop potential solar cells of the future.

“Because of environmental concerns related to nuclear and fossil-fuel-based energy, people are demanding clean alternative energies that can help build up our power grids,” Xu said. “Solar cells are quite safe, but we need to enhance their overall efficiency and affordability. To accomplish this, our group is trying to gain a better understanding of the fundamental processes at work in solar cells.”

The trick is to create cells that are good at both trapping light and generating electricity.

Thick solar cells have properties that are beneficial for capturing light but are inefficient for extraction of electricity and cost more for materials. Thin cells use fewer materials and efficiently generate electricity but are less effective at catching light. Through a nanotechnology process of folding material within the cell, Xu is hoping to create thin cells that are also excellent light catchers.

Xu’s group also is developing novel, environmentally friendly materials that use sunlight as an energy source to burn away organic pollutants from wastewater. The scientists have published a number of journal articles on the topic. Xu hopes the technique could be used for purification of sewage or even oil-contaminated water.

“The CAREER award is a big encouragement for my entire research group, which includes graduate students, undergraduates and research scholars who have been working so hard and intelligently on this project in the past years,” Xu said.

With the new funding, Xu hopes to expand his ongoing research collaboration with Argonne National Laboratory to include more NIU students.

“Energy science is Argonne’s core research area, and I see broadening the collaboration as an effective way to train the next generation of scientists,” Xu said. “NIU students will be exposed to Argonne’s world-class research environment and involved in frontline research projects at a young age. They will also benefit from exposure to scientific teamwork, cutting-edge facilities, cross-disciplinary knowledge and critical-thinking and problem-solving methodologies.”

Xu is the second faculty member in the chemistry and biochemistry department to win a CAREER award from NSF in recent years. Professor James Horn was awarded the grant in 2010 for his research on proteins.

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Chemistry Professor Tao Xu receives CAREER Grant from National Science Foundation

Gareth Denyer wins Life Technologies Education Award

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23 February 2012

Associate Professor Gareth Denyer, from the School of Molecular Bioscience, has won the 2012 Invitrogen Life Technologies Education Award from the Australian Society for Biochemistry and Molecular Biology.

TheInvitrogenLife Technologies Education Award recognises outstanding achievement in education in biochemistry or molecular biology, especially innovation and creativity in education.

Associate Professor Denyerwill receive his award at theComBio conferenceto be held on 23-27 September 2012 at the Adelaide Convention Centre. As part of the award, he will give the main presentation of the Education Symposium at ComBio.

"I'm very humbled to win the Life Technologies Education Award and feel somewhat guilty to get the award because I think that there are several people in my School who are better teachers than me!" said Associate Professor Denyer.

"The buzz that I get from teaching comes from helping students who are struggling. To be the person that enables a student to finally understand a concept that has troubled them for perhaps years is an amazing thing."

Winning the award for his excellent teaching based on his philosophy of focusing on practical teaching outcomes and a minimum of teaching jargon, Associate Professor Denyer is passionate about being creative and experimenting with his teaching. He shows leadership in designing courses, administration and, most recently, the introduction of electronic lab notebooks and student portfolios.

"My teaching philosophy has been shaped by several people who have inspired me and provided guidance along the way in my career, including academics at the University of Oxford where I completed my undergraduate and postgraduate degrees, and here at the University of Sydney, where I have worked for more than 20 years," said Associate Professor Denyer.

"I've been inspired by the various ways that these academics provide a sensitive and inspiring education, so I find the modern trend of judging teachers largely by scholarship and pedagogic research unfortunate. I am passionate about judging teachers by how well they teach.

"Therefore, I am really grateful to theAustralian Society for Biochemistry and Molecular Biologyfor choosing me for the Education Award and I hope it will encourage others who want to enjoy and be effective in their teaching to do so through creativity, experimentation and reflection."

In his presentation at the Education Symposium at ComBio, Associate Professor Denyer will present on his most recent teaching innovations, including the ePortolio/eNotebook, the classes that he and colleagues have set up to build students' confidence in criticising the research literature, the anti-plagiarism solutions that they use in exams and the narrated meta-lectures which provide commentaries on lectures similar to the producer commentaries that come with a movie DVD.

As part of the Invitrogen Life Technologies Education Award, he will also be sent to an international conference of his choice with a significant focus on education.

"I am hoping to attend the conference associated with the ePortfolio system that we are using as a surrogate electronic Lab Notebook. I hope to be able to convince the authors of that software to make changes that will enable the ePortolio system to work as a modern eNotebook which can be used in many other disciplines and even in the real research lab environment."

Read moreabout the Invitrogen Life Technologies Education Award and other Australian Society for Biochemistry and Molecular Biology awards on the Australian Society for Biochemistry and Molecular Biology website.

Media enquiries: Katynna Gill, 02 9351 6997, katynna.gill@sydney.edu.au

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Research and Markets: Pathophysiology, Pharmacology and Biochemistry of Dyskinesia

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DUBLIN--(BUSINESS WIRE)--

Research and Markets (http://www.researchandmarkets.com/research/ad0c22/pathophysiology_p) has announced the addition of Elsevier Science and Technology's new report "Pathophysiology, pharmacology and biochemistry of dyskinesia" to their offering.

Published since 1959, International Review of Neurobiology is a well-known series appealing to neuroscientists, clinicians, psychologists, physiologists, and pharmacologists. Led by an internationally renowned editorial board, this important serial publishes both eclectic volumes made up of timely reviews and thematic volumes that focus on recent progress in a specific area of neurobiology research. This volume reviews existing theories and current research surrounding the movement disorder Dyskinesia. Key Features

Leading authors review state-of-the-art in their field of investigation and provide their views and perspectives for future research Chapters are extensively referenced to provide readers with a comprehensive list of resources on the topics covered All chapters include comprehensive background information and are written in a clear form that is also accessible to the non-specialist

Topics Covered:

An introduction to dyskinesia: the clinical spectrum L-dopa induced dyskinesia - clinical presentation, genetics and treatment Experimental models of LID Mechanisms underlying LID Novel approaches to therapy Surgical approaches to LID Tardive dyskinesia - clinical presentation and treatment Epidemiology and risk factors for TD Genetics of TD Heon Experimental models of TD Surgical approaches to TD Huntington's chorea - clinical presentation and treatment Genetics and pathology of HD Pathogenic mechanisms in HD Experimental models of HD and novel therapeutic approaches Cell based treatments for HD Clinical phenomenology of dystonia Genetics and pharmacological treatment of dystonia Experimental models of dystonia Surgical treatment of dystonia

For more information visit http://www.researchandmarkets.com/research/ad0c22/pathophysiology_p

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Research and Markets: Pathophysiology, Pharmacology and Biochemistry of Dyskinesia

New science can help guide diets and exercise

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The most important weight-loss message - you have to use more calories than you eat - hasn't changed in decades.

But dieting experts say science has some new, surprising things to say about the other half of the standard recommendation - exercise - and about which diet to use.

Researchers are also refining the behavioral tricks that can change the way people eat, not only to lose weight but also to keep it off. Modern technology is giving dieters new options, such as Internet- and cell-phone-based programs or scales that can transmit your weight from your home to your doctor or dietitian.

Thomas Wadden, director of the Center for Weight and Eating Disorders at the University of Pennsylvania, said the last decade has seen "pretty aggressive diet wars" among the proponents of low-fat, low-carb, or low-glycemic-index approaches.

After years of comparisons, Wadden and other experts said the verdict is clear: What you choose doesn't matter. Pick a diet you can stick to, including liquid diets or prepared meals. If you follow the rules, the results are all about the same. Wadden said he does recommend that, whatever the diet, patients reduce saturated fats and trans-fats for better health. You can pick a more aggressive approach while you're losing, eventually transitioning to a diet rich in vegetables, fruits, and lean protein for maintenance.

Gary Foster, director of Temple University's Center for Obesity Research, thinks diet gurus have scared people off with too much information. "We tell people so much stuff, it's paralyzing," he said.

He agreed that the specific diet doesn't matter. "Calories drive weight loss," he said.

To lose a pound a week, a dieter needs to eat 500 fewer calories a day. That's simple enough, but your maintenance needs come down as people get smaller. That explains why weight loss gets harder as you go. Think of your body as a house. It takes more energy to heat a big house than a small one. A woman who weighs 300 pounds maintains her weight on about 3,000 calories. (Because they have more muscle, men use a few more.) A woman who weighs 140 needs only 2,050 calories to stay there. Caloric needs drop further as we age and lose muscle mass.

Cheryl Marco, a registered dietitian who runs Thomas Jefferson University's weight management program, starts patients on a prepackaged diet that includes shakes and bars. Dieters have few options.

"Fewer choices work better," Marco said. "What works is the narrowing of stimuli." So her most successful long-term dieters eat meals that don't vary much from day to day.

Some people may just have to stay away from foods that trigger overeating.

"I am not of the belief . . . that we have the ability to learn to eat high-risk foods in moderation," Marco said. Your high-risk food may be ice cream. Someone else's may be fettuccine Alfredo.

John McAroy, 38, dropped 70 pounds (from 300 on a 6-foot-2 frame) between Thanksgiving and early February using Marco's method. He hasn't cheated much and hasn't missed having more choices. "You'd be surprised," he said. "I'm rarely hungry."

So what about exercise? Isn't it the answer?

No, the experts said.

Exercise is "the single best predictor of who keeps weight off and who doesn't," Foster said. "It has very little effect on weight loss."

Exercise can help people lose weight, but so slowly that most people lose interest, he said. It's easier for most people to cut 500 calories out of their diet a day than to burn an extra 500 calories. You have to walk five miles to do that.

What exercise does do is help people maintain muscle mass, which revs up metabolism a little and improves overall health. Still, adding five pounds of muscle takes a lot of work, and a pound of muscle burns only about 15 calories a day.

In one of the cruel twists of our evolutionary history - the one that shaped our bodies to withstand famine, not a world full of junk food - people who have lost a lot of weight burn fewer calories during exercise than people who have never dieted. "It's as if your body's gone green on you," Wadden said. To keep weight off, dieters need to exercise 225 to 300 minutes a week: about 32 to 43 minutes a day.

Foster's group is looking at whether getting a good night's sleep affects weight loss. People who weigh more tend to sleep less, but it's not yet known whether sleeping more helps people lose weight.

On the behavioral front, researchers say that "accountability" is a crucial factor in making diets work. People do best when they keep track of what they eat and how much they exercise. They need to weigh themselves frequently, ideally every day. It also helps a lot to report what they're doing to someone else. The gold standard is a face-to-face meeting, but results also improve with telephone and Internet reporting.

"It's really important to be accountable to somebody else," Foster said.

It's also important to act quickly when the numbers on the scale start moving up. Experts recommend having an action plan when weight rises by two to four pounds - perhaps returning to more intensive monitoring of food intake - and when dieters fall off the wagon.

"One of the major differences between the average-weight person and the overweight person is the ability to recover from overeating," Marco said.

Wadden says technology is offering new alternatives to people who need to lose weight. While not yet in wide use for weight control, scales that transmit weights to doctors or diet programs can build in accountability. Internet- and phone-based programs make it easier to calculate calories and energy usage.

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New science can help guide diets and exercise

Panasonic Announces Relationship With AAG Health & Wellness Featuring the CardioHealth® Station

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SECAUCUS, N.J. and MIAMI, Feb. 22, 2012 /PRNewswire/ -- Panasonic Healthcare Group and CardioNexus Corporation announced today that they will outfit AAG Health & Wellness practices with the Panasonic CardioHealth Station. A leading Age Management and Hormone Replacement Therapy Center in the United States, AAG Health & Wellness will utilize the Panasonic CardioHealth Station, one of the latest ultrasound medical technologies, in their locations across the nation to support early heart disease detection and enhance their age management medicine programs.

The Panasonic CardioHealth Station is designed to assist medical professionals in making a quick and valuable assessment of cardiovascular health and has been cleared by the FDA for use in the automated acquisition of carotid artery intima-media thickness to help ascertain cardiovascular risk. The Panasonic CardioHealth Station continues to gain the attention of preventive medical professionals, like AAG Health, who recognize that the best ways to reduce long-term healthcare costs is to apply cutting-edge technology to detect signs of disease at an early stage. 

"AAG Health is proud to announce the acquisition of Panasonic's newest offering which provides our patients with the latest in diagnostic testing. AAG Health's Age Management, Healthy Aging and Hormone Treatment programs will incorporate the Panasonic CardioHealth Station as part of our comprehensive and executive level medical health assessments," said Mark White, CEO of AAG Health & Wellness.  "CardioNexus Corporation, the sales arm for Panasonic's CardioHealth Station, has installed this revolutionary device here at AAG Health and has provided comprehensive staff training to ensure the success of our new cardiovascular risk assessment and treatment program which includes complete diagnostic health testing, hormone optimization, anti-aging vitamin supplementation, nutritional counseling and exercise protocols. The Panasonic CardioHealth Station cardiovascular risk assessments will greatly assist our age management medicine physicians with diagnoses and formulating preventative measures to ensure healthy aging for our patients."

"The recent Million Hearts national initiative from the Center for Disease Control has helped shed light on two of the leading causes of death in the United States, heart disease and stroke.  February is American Heart Month, so even greater awareness will surround this initiative and the treatment and prevention of heart disease," said Steven Lynum, Director-Clinical Products, Panasonic Healthcare Group. "The efforts of medical professionals, like those at AAG Health & Wellness, will help to contribute in the campaign's initiative to prevent one million heart attacks and strokes over the next five years and Panasonic is proud to play a part in this national effort with our CardioHealth Station."

About Panasonic Healthcare Group
Based in Secaucus, NJ Panasonic Healthcare Group is a business group of Panasonic Corporation of North America.  Bringing together Panasonic's expertise in a wide range of health and medical device technologies the business unit develops products for the healthcare industry relating to hearing care and diagnostic machines.  For more information visit http://www.panasonic.com/cardiohealthstation or http://www.panasonic.com/business/medicalvideo/hearing-aids/index.asp

About Panasonic Corporation of North America
Based in Secaucus, NJ, Panasonic Corporation of North America provides a broad line of digital and other electronics products for consumer, business and industrial use. The company is the principal North American subsidiary of Osaka, Japan-based Panasonic Corporation (NYSE: PC - News), and the hub of Panasonic's U.S. branding, marketing, sales, service and R&D operations. Panasonic recently announced that it will relocate its North American headquarters to Newark, NJ in 2013 as part of is plans to reduce the size of its carbon emissions footprint. Information about Panasonic and its products is available at http://www.panasonic.com and its Full HD 3D site at http://www.panasonic.com/3D. Additional company information for journalists is also available at http://www.panasonic.com/pressroom.

About the CardioNexus Corporation
Founded on January 2009 in Houston Texas, CardioNexus Corporation is an authorized distributor of Panasonic Healthcare Group. CardioNexus focuses on early detection of cardiovascular disease using an innovative multi-modality approach. Panasonic Corporation of North America became a shareholder of CardioNexus Corporation in October 2010. For more information, visit the company's website at http://www.cardionexus.com.

About AAG Health & Wellness – The Leaders in Hormone Replacement
AAG Health & Wellness is the leading provider of age management medical services, stem cell and hormone replacement therapy for men and women in the United States. AAG Health has a network of over 25 medical health centers throughout the United States. For more information, visit http://www.aaghealth.com

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Panasonic Announces Relationship With AAG Health & Wellness Featuring the CardioHealth® Station

Anti-Aging Protein Extends Life Span in Mice, and Maybe Humans

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Things are looking up for aging mice and, if this research pays off, for aging humans, too.

Researchers have found that a long-suspected anti-aging protein called sirtuin can make male mice live about 16 percent longer than average, the first such advance for mammals in a field that has thus far only offered the blessings of extended life span to yeast, nematodes and fruit flies.

The findings, by scientists at Bar-Ilan University in Israel, appear today (Feb. 22) online in the journal Nature.

Although the Israeli scientists cannot explain why female mice didn't also live longer like the males, an accompanying commentary describes the findings as bringing the field of anti-aging research to a new level of maturity.

Long road to SIRT6

Sirtuin was hot news in 1999 when researchers found that a certain sirtuin called Sir2 could extend life span in yeast by 30 percent. That was about five lifetimes ago for your typical mouse, though. Studies that followed on worms and flies have had mixed results, and some researchers have started to question whether sirtuins could control life span in more complicated life forms.

Mammals, including humans, have seven types of sirtuins, called SIRT1 to SIRT7. Scientists aren't sure what these proteins do, although there is some evidence suggesting that they might help prevent chronic diseases such as cancer and cardiovascular disease. For example, resveratrol, the nutrient found in grape skins (and red wine), has been shown to have a positive effect on heart health, and it may work by activating the SIRT1 gene to make more SIRT1 protein.

The Israeli researchers, led by Yariv Kanfi, focused on SIRT6. The team's previous work revealed that mice genetically bred to have lots of SIRT6 could get fat on rich diets yet show no signs of heart disease, fatty liver disease and other diseases associated with obesity. Previous research by other groups showed that mice genetically bred to have little SIRT6 don't live very long. And, conversely, rats living longer on a calorie-restricted diet have increased levels of SIRT6 in their blood.

So, this time the Israeli team simply decided to let the SIRT6 mice live a natural life. These male mice lived longer, about 16 percent longer on average, than regular mice kept in the same conditions. The female mice with the SIRT6 gene enhancement didn't live longer than regular mice. The researchers speculate that, considering how male mice have a higher rate of cancers compared with the females, the SIRT6 could be acting as a tumor suppressor and thus have a larger effect on male life span than female life span.

Got some time?

It could be that SIRT6 is to mice (and humans) as Sir2 is to yeast, a regulator of life span. Given the title of the Nature study, "The sirtuin SIRT6 regulates lifespan in male mice," that's what the researchers are hoping. [Scientific Tips for a Longer Life]

David Lombard and Richard Miller of the University of Michigan School of Medicine, in an accompanying News and Views article, remain positive yet generally skeptical. They note that measuring life spans in longer-lived and more complex animals can be tricky, because, for example, life spans can vary by many months for genetically similar mice in similar environments with similar feed. The current study used 245 mice, but ultimately may need thousands of mice to produce more reliable statistics.

Meanwhile, questions abound for sirtuin researchers: How is SIRT6 affecting life span at the cellular level? Why are the effects more pronounced in males than females? And how can one activate the SIRT6 gene to make more SIRT6 without the unpleasantness of a caloric-restriction diet?

This could take years to unravel. But better to be a human than a mouse.

Christopher Wanjek is the author of the books "Bad Medicine" and "Food At Work." His column, Bad Medicine, appears regularly on LiveScience.

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Anti-Aging Protein Extends Life Span in Mice, and Maybe Humans